A Freeze on Tailored Antiplatelet Therapy?
It is widely known that there is interindividual variation in the response to aspirin and clopidogrel, drugs that represent two major classes of antiplatelet therapies in use today. Variation in response can be defined clinically, i.e., not all patients who are exposed to the drug are protected from platelet-mediated thrombotic events such as myocardial infarction (MI). Response can also be defined pharmacodynamically in the laboratory employing ex vivo measures of platelet inhibition such as the VerifyNow® platform- a whole blood, point-of-care test. A rich history of epidemiologic and genetic data demonstrates an association between variability in laboratory responses and clinical outcomes among patients receiving antiplatelet therapy. To test the hypothesis that measures of ex vivo platelet function are truly risk factors and not merely risk markers, the ARCTIC study randomly assigned patients undergoing percutaneous coronary intervention (PCI) to a strategy of platelet function testing and subsequent adjustment of antiplatelet therapy vs. usual care. The primary results from ARCTIC failed to demonstrate a benefit from incorporating platelet function test results into management of antiplatelet therapies in this population.1 In a secondary analysis published in this issue of Circulation2, the ARCTIC investigators assessed the extent to which outcomes differed after hospital discharge by performing a landmark analysis. Similar to the previously reported primary findings, a strategy of platelet function test-driven treatment changes did not affect clinical outcomes from the time of discharge through the end of follow up. Although the question asked is sound and of potential clinical relevance, many unanswered questions remain to better determine in whom and under what conditions a strategy of tailored antiplatelet therapy may improve clinical outcomes.
- Received April 4, 2014.
- Accepted April 8, 2014.